Hyponatremia

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Hyponatremia

• Anthony R Mato, MD

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Remember the basics of the bodys fluid
compartments.

• TBW WEIGHT x .5 (women) or .6 (men)
• TBW x 1/3 ECF
• TBW x 2/3 ICF
• ECF x 2/3 Interstitial compartment
• ECF x 1/4 Intravascular compartment
• Water will move freely to balance osmolalities
  Therefore all compartments have equal
  osmolalities.
• Sodium is the major extracellular cation.

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King Sodium Rules the ECFV

• The total amount of Na in the ECF is the main
  determinant of the size of the ECFV.
• If ECF Na increases so will the ECFV.
• The edematous states CHF, liver cirrhosis, and
  nephrotic syndrome are examples of increased
  total body Na in the extracellular compartment
  causing volume overload.

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ECFV overload results from too much sodium in the
ECF compartment. ECFV depletion results from too
little sodium in the ECF compartment.
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The Axis of Sodium

• The kidney controls the size of the ECFV by
  controlling Na excretion.
• Kidney is programmed to keep the ECFV within an
  acceptable range. The kidney will use 3 systems
  to regulate ECFV (afferent sensory arm to sense
  ECFV and efferent arm to effect change).
• Renin AT II Aldosterone axis
• ANP system
• Sympathetic nervous system

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Its NOT IMPORTANT TO MEMORIZE THE PATHWAYS.
IMPORTANT TO KNOW that when ECFV increases
mechanisms are triggered to excrete Na as the
response. When ECFV decreases mechanisms are
triggered to retain Na as the response.
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NOTE THAT WE HAVE NOT YET MENTIONED THE CLINICAL
MEASURE OF SODIUM CONCENTRATION. Na is a
measure of Na relative to water. It tells you
NOTHING about the total body sodium.
Abnormalities in the Na concentration tell us
that there are abnormalities in the amount of
WATER in the ECF compartment.
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THINK H20
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THINK H20
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Think H20
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Osmolality vs. Tonicity

• Osmolality total solute concentration in a fluid
  compartment.
• Tonicity the combined ability of solutes to
  produce a osmotic driving force that causes water
  to move from one compartment to another.
• Solutes that are capable of moving water are
  called effective osmoles.
• These are solutes that are unable to cross from
  the extracellular to the intracellular
  compartment sodium, glucose, mannitol, sorbitol.
  NOT UREA. 
• The control of tonicity will determine the normal
  state of cellular hydration and cell size. This
  is of particular concern in the case of brain
  cells.

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Na (tonicity) can make water move!
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Osmolality

• Osmolality Osmoles/kg of water
• 2(Na) Glucose/18 BUN/2.8
• Normal is 285-295

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To regulate water excretion and keep the tonicity
(Na concentration) of ECFV constant there must
be

• Adequate GFR.
• Delivery of GF to the concentrating and diluting
  segments of the loop of Henle and distal nephron.
  
• Intact tubular concentrating and diluting
  mechanisms,
• Appropriate turning on/off of ADH.
• ADH responsiveness of the kidney.

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ALL OF THE CLINICAL DISORDERS PRODUCING HYPER AND
HYPONATREMIA MAY BE UNDERSTOOD AND REMEMBERED
BASED ON ABNORMALITIES OF THESE MECHANISMS.
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A Note on Diuretics

• Both loop and thiazide diuretics block the
  reabsorption of Na and can therefore can lead to
  a decrease in the size of the ECFV.
• They DIFFER in that loops produce a balanced loss
  of Na and Water ? therefore Na concentration is
  usually undisturbed.
• Thiazide causes an unbalanced loss of Na and
  Water such that more Na is lost relative to
  water causing hyponatremia.

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The Body Has Simple Goals

•  Goals of the body
• Maintain Na concentration within a narrow range.
• Maintain ECFV within an acceptable range.

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Volume Status is a Na Problem

• IN CLINICAL PRACTICE, IT IS MOST USEFUL TO
  CONSIDER THAT CASES OF ABNORMAL ECFV SIZE ARE DUE
  TO PROBLEMS WITH THE CONTROL MECHANISMS
  regulating TOTAL BODY SODIUM.
• Ask yourself, how might the Na mechanisms be
  impaired.
• Volume overload can be viewed as being total body
  Na overloaded.
• Volume depletion can be viewed as having too
  little total body body Na.

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Sodium is a water problem.

• IN CLINICAL PRACTICE, IT IS MOST USEFUL TO
  CONSIDER THAT CASES OF ABNORMAL ECF SODIUM
  CONCENTRATION ARE DUE TO PROBLEMS WITH THE WATER
  CONTROL MECHANISMS.  
• Ask yourself, how might water controlling
  mechanisms be impaired.
• This is where the diagnosis and treatment must
  focus.

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ATTACK VOLUME AND SODIUM CONCENTRATION AS TWO
SEPARATE PROBLEMS. THIS TABLE WILL HELP BREAK IT
DOWN.
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Causes of Hyponatremia most cases will by the
hypotonic, hypoosmolar state.

• Pseudohyponatremia Na is low, but serum osm is
  normal. This value is an artifact due to the
  accumulation of other plasma constituents in
  plasma hypertriglyceridemia, hyperproteinemia
  (MM).
• Here measured osm are normal but the calculated
  osm will be low (low Na).
• The patient will be asymptomatic since the
  tonicity is normal.
• This is rare now since the Na electrode method is
  used to measure serum Na.

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Causes of Hyponatremia most cases will by the
hypotonic, hypoosmolar state.

• Hyponatremia with hypertonicity Na is low
  since water will flow into the ECF compartment as
  a result of hyperglycemia for example.
• The calculated and measured osm will be elevated
  in that case. Na will decrease by approx 1.6
  meq/dL for every 100 mg/dl increase in glucose
  above 100.
• In the case of mannitol the measured osm will be
  high but the calculated osm will be low.

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Hyponatremia with hypotonicity impaired renal
water excretion in the setting of continued water
intake. THE REASON WHY THE KIDNEY CAN NOT
CONCENTRATE THE URINE IS THE KEY TO DIAGNOSING
THE CAUSE OF HYPONATREMIA.
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Use your physiology to figure it out. March down
the nephron.

• Impaired GFR if one cannot filter a water load
  then one cannot excrete a water load. At GFR of
  lt 20 we start to have problems with water
  handling.
• ECFV depletion gastric losses with water
  depletion. Proximal tubule is the culprit
  solvent drag.
• Edematous states These people have abnormal
  retention of Na and water. CHF, liver, nephrotic
  disease.

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Use your physiology to figure it out. March down
the nephron.

• Thiazide diuretics block the kidneys ability to
  produce a dilute urine.
• SIADH pituitary release, ectopic production,
  ADH-like meds, potentiation effects of meds on
  ADH action at the renal tubule.
• Endocrine Hypothyroidism and Hypoadrenalism.
• You cant make a concentrated urine if you do not
  have an adequate solute intake. These patients
  are usually elderly and have a decreased osm
  excretion. Tea and Toast.
• Beer drinkers also take in large amounts of
  fluids with a relatively low solute load.

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Treatment

• The rapidity of the development of hyponatremia
  is more important than the actual value of the
  serum sodium concentration.
• In the chronic / slow setting the cells have time
  to transport intracellular solutes to the
  extracellular space to account for the
  hypotonicity of the extracellular space.
• If this is corrected rapidly osmotic
  demyelination syndrome can occur.
• The most severe form of ODS will be quadriplegia
  (the locked in syndrome).

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Chronic Hyponatremia

• Keep in mind that to develop progressive
  hyponatremia you need an impairment of water
  excretion as well as continued water intake.
  (ESRD patient).
• Before you diagnose a specific etiology you can
  always restrict free water intake to 800 cc / day
  as a temporizing / stabilizing measure

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Volume overloaded states

• Water restriction is also the appropriate
  treatment for hyponatremia.
• This will deal with the water excretion problem
  and loop diuretics will deal with the
  hypervolemia state (sodium overload problem).
• Thiazides can acutely worsen the situation.
• IF THERE IS NO HYPONATREMIA IN THE VOLUME
  OVERLOAED STATE THEN THERE IS NO NEED TO RESTRICT
  WATER.
• IF EDEMA IS THE SOLE PROBLEM THEN IT IS A PROBLEM
  OF SODIUM EXCRETION AND YOU WILL NEED TO
  INCREASE SODIUM EXCRETION AND RESTRICT SODIUM
  INTAKE.

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ECFV Depletion The Vomiting Patient

• In ECFV depletion you have a water and sodium
  problem.
• Urine sodium will be low.
• Urine Na will also be low in the hypervolemic
  states as well.
• These people will usually respond to NS.
• Physiologically the culprit is the proximal
  tubule.

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SIADH Treatment

• Water restriction.
• NaCl tablets (as a solute load)
• Demclocycline.
• ADH receptor antagonists (The future?)
• Find the underlying cause of the hyper ADH state.

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Acute / Symptomatic Hyponatremia

• Correct Na no faster than 1 meq / L per hour
  until achieving a 6-8 meq / L increase, then .5
  meq / L / hour or less.
• Permit no more than 10-12 meq/ L increase in Na
  over 1st 24 hours.
• Slow or stop infusions when symptoms improve.
• The goal is not correct the serum sodium, but to
  correct the cerebral edema.

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How to use 3 Saline.

• Sodium deficit Na desired Na measured x TBW
• 513 meq Na in 1 L of 3 saline Sodium deficit /
  513 will give you the volume to infuse.
• Set the rate.
• This should be done with the guidance of renal
  medicine. This should be done in an ICU setting.
  
• Once we have treated the symptoms we can stop
  this dangerous drug and start more conservative
  measures as treatment.

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PUTTING IT ALL TOGETHER
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An Alternative Approach.
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Clinical Cases
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Adheesh

• 23 yr old male develops watery diarrhea. He
  comes to your ER lightheaded and orthostatic. He
  has dry MM and tachycardia. Neuro exam is normal
  and he is alert.
• Labs Na 129, K 3, HCO3 20, BUN 20, Cr 1,
  Glucose 75, Urine Na 5, Urine osm 520.

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Adheesh

• What is serum OSM?
• What is volume status?
• Is the volume loss renal / extra renal?
• What is the cause of the hyponatremia?
• How would you treat this patient?

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I ran out of insulin case
72 yr old woman with DM presents to ER with
polyuria and polydipsia x 5 days. PE is normal.
Labs Na 129, K 4.2, Cl 89, HC)3 24, BUN 5,
Cr.08, Glucose 780. What is the osm? Why is he
hyponatremic? What is the corrected Na? What is
the treatment?
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Unresponsive A Na emergency
38 yr old woman with Hep C is brought to ED
unresponsive. She is obtunded with elevated JVP,
rales b/l, massive ascites, and 2 edema.
Labs Na 112, K 4.1, Cl 89, HCO3 24, BUN 32, Cr
.7, Glucose 90, Urine Na 2, Urine OSM 800. What
is the osm? What is the volume status? Why is she
hyponatremic? What is the treatment(s)?
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Case 1
You are called as a curbside consult for an
outpatient hyponatremia case. Serum Na is 120.
Pt is asymptomatic. Other data Cl 80, K 4.5,
HCO3 24, BUN 14, glucose 90. What further
questions do you ask?
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Case 2
A 50 yr old male with h/o hyperlipidemia has the
following labs Na 125, M-Osm 270, TGs 1000,
total protein 8.5. The blood is lipemic. Is this
a case of pseudohyponatremia?
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Case 3
Mr. T has 3 days of N/V, polyuria and polydipsia.
Exam poor turgor and orthostatic. Labs glucose
360, Na 120, BUN 28. M-OSM 270. What is the cause
of this hyponatremia? What will Na be once
glucose is corrected to 100?
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Case 4
Mrs. NA has polyuria, polydipsia, and delta MS.
Exam shows poor turgor and orthostasis. Labs
glucose 2100, Na 130, BUN 40. M-OSM 395. What
is the cause of the hyponatremia? What will Na be
once glucose is corrected? What fluid should you
use?
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Case 5
Mr. JD comes to the ER staggering and smelling
foul. Na is 140, glucose 180, and BUN 28. M-OSM
330. What is your diagnosis? How could you
confirm it using the above lab data?
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Case 6
RR has a classic exam in addition to his new
onset edema after eating some chips. He has
elevated JVP, crackles, S3. CXR shows b/l
pulmonary edema. Labs Na 125, urine Na 5, M OSM
270. Why is serum Na low? How would you treat
this?
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Case 7
RR return to clinic in florid CHF. This time his
Na is 138. What treatments would you now offer
him?
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Case 8
Jenny a 46 yr old female presents with N/V and
abdominal pain. MM are dry, skin has poor turgor,
and she is orthostatic. She notes a h/o
PUD. Labs Na 125, U Na 5, M OSM 270. What is
happening? What therapy do you implement?
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Case 9
72 yr old male who is a heavy smoker presents
with cough and hemoptysis. His physical exam is
completely normal in terms of volume status. CXR
reveals a 6 cm left sided chest mass. Labs Na
125, K 4.2, Cr 1.1, M OSM 270, Urine Na is 45. He
takes no meds. TSH and am cortisol are normal.
What is causing the hyponatremia?
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Case 10
50 yr old 60 kg advertising executive is
recovering from TOA surgery. She has been getting
D5 ½ NS x 36 hours. You are called s/p a seizure
preceded by confusion. You send off the stat labs
and find Na 116 (baseline 136), M OSM 258. What
has happened? What do you do?
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Case 11
A man with SIADH has a fixed urine osm of 600
mosm/L. Solute excretion is measured to be 600
mosm/day. What amount of water could he safely
drink? What could you do to improve this to a
more reasonable amount?